Leicester University has found that the protein RBM3 helps restore brain
activity when animals wake up from hibernation, and could be a treatmement
for people with dementia

A protein which protects hibernating animals during lengthy spells of sleeping could be the key to fighting Alzheimer’s disease, scientists believe.

The University of Leicester has discovered that a ‘cold-shock’ protein is crucial for preventing the loss of brain cells and their connections when body temperature drops to dangerous levels.

When animals hibernate the number of brain cell links - known as synapses - decreases, allowing them to enter a state of torpor.

Scientists have found that the protein RBM3 helps synapses to rebuild once the animal wakes, restoring normal brain activity.

Humans also have the protein, but it appears not to function in people with Alzheimer's disease. The researchers are hopeful that a drug which mimics or increases its effect could help restore lost brain functions for people with dementia.

A state of hypothermia is known to protect the brain. People have been survived for hours after a cardiac arrest without brain damage after falling into icy water.

Similiarly, cooling the brains of babies that have suffered a loss of oxygen at birth is also used to protect against brain damage.

In the study researchers reduced the body temperature of mice with Alzheimer’s disease and a healthy control group to 16-18ºC – similar to the temperature of a hibernating small mammal – for 45 minutes. They discovered that the RBM3 protein kicked in for the healthy animals and helped restore function when they warmed up. However the protein appeared not to function for the mice with Alzheimer's.

“We’ve known for some time that cooling can slow down or even prevent damage to brain cells, but reducing body temperature is rarely feasible in practice: it’s unpleasant and involves risks such as pneumonia and blood clots," said Professor Giovanna Mallucci, who led the research team, at the Medical Research Councils Toxicology Unit at the University of Leicester.

“But, by identifying how cooling activates a process that prevents the loss of brain cells, we can now work towards finding a means to develop drugs that might mimic the protective effects of cold on the brain.”

Professor Hugh Perry, chairman of the MRC’s Neurosciences and Mental Health Board, which funded the research, said: “The neuroprotective pathway identified in this study could be an important step forward. We now need to find something to reproduce the effect of brain cooling. Just as anti-inflammatory drugs are preferable to cold baths in bringing down a high temperature, we need to find drugs which can induce the effects of hibernation and hypothermia.”

The research, which was published in the journal Nature, was welcomed by chairites.

Dr Doug Brown, Director of Research and Development at Alzheimer’s Society said: “We know that cooling body temperate can protect the brain from some forms of damage and this method is being investigated as a treatment for acute conditions such as strokes and brain injury.

“It’s interesting to see this protective mechanism now also being studied in neurodegenerative disease.”